Optic neuritis: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*The exact pathogenesis of | *The exact [[pathogenesis]] of optic neuritis is not completely understood. | ||
*It is | * But It is likely due to some [[inflammatory]] process which leads to delayed type IV [[hypersensitivity]] reaction induced by released [[Cytokines|cytokine]]<nowiki/>s and other inflammatory mediators from activated peripheral [[T-cells]] which can cross the [[blood brain barrier]] and cause destruction of [[myelin]], neural [[cell death]] and [[Axonal|axonal degeneration]]. | ||
* In addition to involvement of the [[myelin sheath]] ([[white matter]]), latest technologies such as [[optical coherence tomography]] (OCT) suggest involvement of [[axons]] ([[Gray matter|gray matte]]<nowiki/>r) in this process. | |||
* | |||
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host. | *[Pathogen name] is usually transmitted via the [transmission route] route to the human host. | ||
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. | *Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. | ||
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On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | ||
Permanent visual loss (40%to 60%) and visual deficit in ON is a result of axonal loss in the optic nerve and retina and corresponding retinal nerve fiber layer (RNFL) thinning, in addition to conduction block caused by demyelination of the optic nerve [8,14,15]. | Permanent visual loss (40%to 60%) and visual deficit in ON is a result of axonal loss in the optic nerve and retina and corresponding retinal nerve fiber layer (RNFL) thinning, in addition to conduction block caused by demyelination of the optic nerve [8,14,15]. | ||
Revision as of 15:17, 7 November 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Historical Perspective
Discovery
- Optic neuritis was first discovered by von Graefe and Nettleship, in late nineteenth century when ophthalmoscopy became part of the ophthalmic examination.[1]
- The association between systemic sclerosis and optic neuritis was made by the early 1900's but there was much controversy and misunderstanding about its differential diagnosis, pathogenesis, and possible treatment.[1]
- Optic neuritis was first distinguished from infectious,hereditary, toxic, nutritional, and ischemic optic neuropathies during the twentieth century.[1]
- During late twentieth century, the development of MRI and the results from recent clinical trials, discovered the relationship between optic neuritis and multiple sclerosis.[1]
Classification
Optic neuritis may be classified into atypical or typical subtypes based on its clinical features.[2]
- Atypical optic neuritis entails clinical manifestations that deviate from classic pattern of optic neuritis features.[3]
- Atypical features to consider include:[3]
- Lack of pain
- Simultaneous or near-simultaneous onset
- Lack of response to or relapse upon tapering from corticosteroids
- Optic neuritis due nerve head or peripapillary hemorrhages
Pathophysiology
Pathogenesis
- The exact pathogenesis of optic neuritis is not completely understood.
- But It is likely due to some inflammatory process which leads to delayed type IV hypersensitivity reaction induced by released cytokines and other inflammatory mediators from activated peripheral T-cells which can cross the blood brain barrier and cause destruction of myelin, neural cell death and axonal degeneration.
- In addition to involvement of the myelin sheath (white matter), latest technologies such as optical coherence tomography (OCT) suggest involvement of axons (gray matter) in this process.
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Permanent visual loss (40%to 60%) and visual deficit in ON is a result of axonal loss in the optic nerve and retina and corresponding retinal nerve fiber layer (RNFL) thinning, in addition to conduction block caused by demyelination of the optic nerve [8,14,15].
Causes
Common Causes
Common causes of [disease name] may include:
- [Cause1]
- [Cause2]
- [Cause3]
Differentiating Optic Neuritis from other Diseases
Epidemiology and Demographics
Optic neuritis typically affects young adults ranging from 18–45 years of age, with a mean age of 30–35 years. There is a strong female predominance. The annual incidence is approximately 5/100,000, with a prevalence estimated to be 115/100,000.[4]
Age
Gender
Race
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Criteria
Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ 1.0 1.1 1.2 1.3 Volpe NJ (December 2001). "Optic neuritis: historical aspects". J Neuroophthalmol. 21 (4): 302–9. PMID 11756864.
- ↑ Kliethermes MA (July 1988). "Working parents in two-pharmacist marriages". Am J Hosp Pharm. 45 (7): 1500. PMID 3414716.
- ↑ 3.0 3.1 Gaier ED, Boudreault K, Rizzo JF, Falardeau J, Cestari DM (December 2015). "Atypical Optic Neuritis". Curr Neurol Neurosci Rep. 15 (12): 76. doi:10.1007/s11910-015-0598-1. PMID 26467052.
- ↑ Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT (1995). "Optic neuritis: a population-based study in Olmsted County, Minnesota". Neurology. 45 (2): 244–50. PMID 7854520.